Central 5-HT<sub>3</sub> Receptor Stimulation by m-CPBG Increases Blood Glucose in Rats

Carvalho, F.; Macedo, Danielle; Bandeira, Isabelle Pastor; Maldonado, Igor Lima; Salles, L; Azevedo, Monalisa F.; Rocha, M.A.; Fregoneze, J.B.; Castro-e-Silva, Emilio De

doi:10.1055/s-2002-20525

Cited by 14 publications

(9 citation statements)

References 18 publications

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“…[47]. It has been shown that administration of ondansetron, a 5-HT 3 receptor antagonist, reduced elevated level of blood glucose in stressed rats stimulated by meta-chlorophenylbiguanide (m-CPBG) [48]. Another report indicated that tropisetron is able to enhance the insulin release in the beta-cell line (INS-1) [49], especially in presence of serotonin.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Rahimian

Zirak

Seyedabadi

et al. 2017

Biomedicine & Pharmacotherapy

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Acute pancreatitis (AP) causes morbidity and mortality. The aim of the present study was to investigate the protective effect of tropisetron against AP induced by cerulein. Cerulein (50μg/kg, 5 doses) was used to induce AP in mice. Six hours after final cerulein injection, animals were decapitated. Hepatic/pancreatic enzymes in the serum, pancreatic content of malondialdehyde (MDA), pro-inflammatory cytokines and myeloperoxidase (MPO) activity were measured. Tropisetron significantly attenuated pancreatic injury markers and decreased the amount of elevated serum amylase, lipase, alanine aminotransferase (ALT), aspartate aminotransferase (AST), MPO activities and pro-inflammatory cytokines levels caused by AP in mice. Tropisetron didn't affect the pancreatic levels of MDA. Our results suggest that tropisetron could attenuate cerulein-induced AP by combating inflammatory signaling. Further clinical studies are needed to confirm its efficacy in patients with AP.

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Section: Discussionmentioning

confidence: 99%

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Rahimian

Zirak

Seyedabadi

et al. 2017

Biomedicine & Pharmacotherapy

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“…OH-DPAT, a selective 5-HT 1A agonist, increases blood glucose levels when administered centrally [33]. Carvalho et al [34] have shown that activation of central 5-HT 3 receptors by the selective agonist m -chlorophenylbiguanide produces hyperglycemia in both fasted and fed rats and that this is blocked by ondansetron. …”

Section: Discussionmentioning

confidence: 99%

Induction of Glucose Intolerance by Acute Administration of Rimonabant

et al. 2012

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Background/Aims: Rimonabant is a cannabinoid CB1 receptor antagonist. Other CB1 antagonists have biphasic effects on blood glucose levels following acute administration. We therefore tested the effects of rimonabant on glucose tolerance following acute administration. Methods: We tested the effects of oral and intracerebroventricular administration of rimonabant on blood glucose and gastrointestinal transit in mice following oral and intravenous glucose challenge. Results: We found a dose-dependent increase in blood glucose from oral doses of rimonabant of 3 mg/kg and above. WIN55,212-2 (3 mg/kg), a cannabinoid receptor agonist, did not influence blood glucose in the presence or absence of rimonabant. Rimonabant did not induce release of glucose from isolated rat hepatocytes or modify serum insulin concentration in mice. Intracerebroventricular administration of rimonabant caused increases in blood glucose and gastrointestinal transit, suggesting a central nervous system site of action. Increases in blood glucose by rimonabant were partially blocked by the dopamine receptor antagonist haloperidol and significantly blocked by the 5-hydroxytryptophan (5-HT) depleting agent p-CPA and the 5-HT₃ receptor antagonist ondansetron. Conclusions: Rimonabant causes a dose-dependent increase in glucose profile upon glucose challenge partially mediated by the central nervous system control of gastrointestinal carbohydrate absorption through pathways that are modulated by both 5-HT and dopamine.

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“…The lack of this higher endogenous CRH−related Quipazine is a serotonergic agonist that stimulates 5−HT 1 , 5−HT 2 and 5−HT 3 receptors. We have previously demonstrated that cen− tral pharmacological activation of 5−HT 3 receptors by the selec− tive agonist m−CPBG increases plasma glucose levels [9]. In the present paper, we have shown that quipazine−induced hypergly− cemia is, at least in part, due to the activation of central 5−HT 3 re− ceptors since pretreatment with two different selective 5−HT 3 antagonists, LY−278,584 and ondansetron, was able to reduce quipazine enhancement of plasma glucose levels.…”

Section: Discussionmentioning

confidence: 99%

“…Also, the central administration of selective 5− HT 2A and 5−HT 2C receptor agonists enhances blood glucose by a mechanism that seems to be dependent on peripheral adrenaline release [7,8]. We have recently shown that pharmacological acti− vation of central 5−HT 3 receptors by the selective agonist m− CPBG provokes a significant increase in blood glucose [9].…”

Section: Introductionmentioning

confidence: 98%

Hyperglycemia Induced by Pharmacological Activation of Central Serotonergic Pathways Depends on the Functional Integrity of Brain CRH System and 5-HT3 Receptors

Carvalho

Barros²,

Silva³

et al. 2005

Horm Metab Res

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In the present study, we investigated the effect of central serotonergic pathway activation achieved through third ventricle injections of quipazine, a serotonergic agonist, on plasma glucose levels of fasted and fed adult Wistar male rats, whose third ventricles were canulated 7 days before the experiments. Central quipazine administration induced a significant increase in plasma glucose levels in fasted animals, but was unable to modify plasma glucose concentrations in fed rats. Pretreatment with alpha-helical CRH, a CRH antagonist, significantly attenuated quipazine-induced hyperglycemia. Pretreatment with two different 5-HT3 receptor antagonists, LY-278,584 and ondansetron, was also able to produce a significant reduction in the hyperglycemic response evoked by central administration of quipazine. None of the antagonists used was capable of modifying plasma glucose concentrations when injected alone into the third ventricle. Quipazine-treated, hyperglycemic animals did not show any increase in plasma insulin levels. We conclude that acute pharmacological serotonergic stimulation by quipazine produces hyperglycemia by mechanisms that require the functional integrity of both CRH and 5-HT3 receptors, and that impairment in insulin secretion and/or activity may explain hyperglycemia induced by third ventricle injections of quipazine.

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Central 5-HT₃ Receptor Stimulation by m-CPBG Increases Blood Glucose in Rats

Cited by 14 publications

References 18 publications

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Induction of Glucose Intolerance by Acute Administration of Rimonabant

Hyperglycemia Induced by Pharmacological Activation of Central Serotonergic Pathways Depends on the Functional Integrity of Brain CRH System and 5-HT3 Receptors

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Central 5-HT3 Receptor Stimulation by m-CPBG Increases Blood Glucose in Rats

Cited by 14 publications

References 18 publications

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Induction of Glucose Intolerance by Acute Administration of Rimonabant

Hyperglycemia Induced by Pharmacological Activation of Central Serotonergic Pathways Depends on the Functional Integrity of Brain CRH System and 5-HT3 Receptors

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Central 5-HT₃ Receptor Stimulation by m-CPBG Increases Blood Glucose in Rats